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Objective: Smad7 was identified as a TGF-β-inducible antagonist of TGF-β signaling and might participate in a negative feedback loop to control TGF-β signaling. In this study, the responsiveness of Smad7 to TGF-β1 was examined in the BEP2D and BERP35T-2 cells to investigate the possible mechanism of Smad7 in the tumorigenesis. Methods: North and west blot were performed to exam the Smad7 and TGF-β1 expression abundance in BEP2D and BERP35T-2 at both transcription and translation level. Results: The expression level of Smad7 mRNA in BERP35T-2 cells was higher than that in BEP2D cells. When stimulated with TGF-β1, Smad7 expression was up-regulated evidently in BEP2D cells, but not significantly in BERP35T-2 cells. The abundance of TGF-β1 in the cytoplasm of BERP35T-2 was not significantly higher than in BEP2D (P>0.05); whereas the abundance of TGF-β1 in BERP35T-2 cell culture medium was significantly higher than in BEP2D cell culture medium (P<0.05). Conclusion: Over expression of Smad7 mRNA and down-regulation of the cells’ responsiveness to TGF-β1 in human lung cancer cell line might be involved in lung carcinogenisis.